Publication

Neuroepigenetic mechanisms in disease

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Last modified
  • 03/05/2025
Type of Material
Authors
    Michael A. Christopher, Emory UniversityStephanie M. Kyle, Emory UniversityDavid J Katz, Emory University
Language
  • English
Date
  • 2017-10-16
Publisher
  • BioMed Central
Publication Version
Copyright Statement
  • © 2017 The Author(s).
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1756-8935
Volume
  • 10
Issue
  • 1
Start Page
  • 47
End Page
  • 47
Grant/Funding Information
  • SMK was supported by the Emory CND training grant (T32NS007480).
  • This work was supported by a grant to DJK from the National Institute of Neurological Disorders and Stroke (1R01NS087142).
  • MAC was supported by the Emory GMB training grant (T32GM008490).
Abstract
  • Epigenetics allows for the inheritance of information in cellular lineages during differentiation, independent of changes to the underlying genetic sequence. This raises the question of whether epigenetic mechanisms also function in post-mitotic neurons. During the long life of the neuron, fluctuations in gene expression allow the cell to pass through stages of differentiation, modulate synaptic activity in response to environmental cues, and fortify the cell through age-related neuroprotective pathways. Emerging evidence suggests that epigenetic mechanisms such as DNA methylation and histone modification permit these dynamic changes in gene expression throughout the life of a neuron. Accordingly, recent studies have revealed the vital importance of epigenetic players in the central nervous system and during neurodegeneration. Here, we provide a review of several of these recent findings, highlighting novel functions for epigenetics in the fields of Rett syndrome, Fragile X syndrome, and Alzheimer's disease research. Together, these discoveries underscore the vital importance of epigenetics in human neurological disorders.
Author Notes
Keywords
Research Categories
  • Biology, General
  • Biology, Molecular
  • Biology, Cell

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